CV-11974, angiotensin II type I receptor antagonist, protects against ischemia–reperfusion injury of the small intestine in rats

Takagi, Tomohisa; Yoshida, Norimasa; Isozaki, Yutaka; Shimozawa, Makoto; Katada, Kazuhiro; Manabe, Hiroki; Hanada, Osamu; Kokura, Satoshi; Naito, Yuji; Okanoue, Takeshi; Yoshikawa, Toshikazu

doi:10.1016/j.ejphar.2006.02.005

Cited by 22 publications

(26 citation statements)

References 37 publications

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“…Furthermore, recent fi ndings indicate that Ang II induces production of ROS through vascular [8,47,48] and neutrophil NADPH oxidases [42], and that the increased production of ROS in turn regulates the subsequent amplifi cation of the proinfl ammatory response in the cell [47,48]. In addition, it has been demonstrated that interfering with Ang II-AT1 pathway (inhibition of ACE or AT1a receptor) offers an anti-infl ammatory effect with respect to the reduced leukocyte-accumulation in the gut [49,50].…”

Section: Discussionmentioning

confidence: 99%

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

et al. 2008

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“…it was previously reported that cinc-1 levels increased during small intestinal i/r injury and that cinc-1 was related to the extent of mucosal damage with neutrophil accumulation (21,22,35). in addition, a previous study demonstrated that pre-treatment with an anti-cinc-1 monoclonal antibody attenuated reperfusion injury in the small intestine, in association with a reduction in TnF-α and MPo levels, thereby prolonging survival (36).…”

Section: A B Bmentioning

confidence: 99%

“…The animals were housed at 22˚C in a controlled environment with 12 h of artificial light per day, and were allowed access to rat chow and water ad libitum. intestinal i/r injury was induced according to the method described in previous studies (21,22). Briefly, the rats were anesthetized with urethane (1 mg/kg, intraperitoneally).…”

Section: Surgical Procedures and Evaluation Of Intestinal Injury Malementioning

confidence: 99%

Proinflammatory role of protease-activated receptor-2 in intestinal ischemia/reperfusion injury in rats

et al. 2010

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Abstract. Protease-activated receptors (Pars) are widely recognized for their modulatory properties during inflammation. The aim of the present study was to examine the role of Par-2 on ischemia/reperfusion-induced small intestinal injury in rats. intestinal damage was induced in male Wistar rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion for 60 min. expression of Par-2 in the intestinal mucosa was estimated by Western blot analysis and real-time Pcr. anti-rat Par-2 cleavage site (PcS) antibody was intraperitoneally administered to the rats 1 h before the vascular clamping. The intestinal mucosal injury and inflammation were evaluated by biochemical markers and histological findings. Thiobarbituric acid (TBa) reactive substances and tissueassociated myeloperoxidase (MPo) activity were measured in the intestinal mucosa as indices of lipid peroxidation and neutrophil infiltration, respectively. Expression of cytokineinduced neutrophil chemoattractant-1 (cinc-1) in intestinal mucosa was measured by enzyme-linked immunosorbent assay. expression of Par-2 mrna and protein in the intestinal mucosa was increased after reperfusion following ischemia. reperfusion after ischemia resulted in an increase in luminal protein concentrations, hemoglobin concentrations, TBa reactive substances, MPo activity and cinc-1 protein.Pre-treatment with anti-rat PCS antibody significantly inhibited the increases in these parameters. These results suggest that Par-2 plays an important role in the pathogenesis of ischemia/reperfusion-induced intestinal injury.

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“…Functional AT1Rs have been found in the rat ileum and duodenum (34). Other studies have shown that the AT1R antagonist inhibited the development of intestinal mucosal injury induced by ischemia-reperfusion in rats (40). Furthermore, ACE-I inhibition, which decreases the production of angiotensin II, has been shown to decrease postischemic injury (14, 26a, 28).…”

Section: Discussionmentioning

confidence: 94%

“…Ang II also stimulates a wide variety of proinflammatory responses including increased leukocyte rolling and adhesion, production of oxidative stress, and induction of cysteine-x-cysteine chemokine expression (3,28,47). It has been shown that the Ang II subtype-1 receptor (AT1R) antagonist significantly inhibits the intestinal mucosal injury induced by ischemia-reperfusion in rats (40). The AT1R mediates many biological effects of the renin-angiotensin system (RAS), such as vasoconstriction, water and sodium retention, free radical release, and cell growth (9).…”

mentioning

confidence: 99%

Estrogen prevents intestinal inflammation after trauma-hemorrhage via downregulation of angiotensin II and angiotensin II subtype I receptor

Chen¹,

Yang²,

Hu³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Although angiotensin II (Ang II) plays a key role in development of organ ischemia-reperfusion injury, it remains unclear whether it is involved in development of intestinal injury following trauma-hemorrhage (T-H). Studies have shown that 17β-estradiol (E2) administration following T-H improves small intestinal blood flow; however, it is unclear whether Ang II plays a role in this E2-mediated salutary effect. Male Sprague-Dawley rats underwent laparotomy and hemorrhagic shock (removal of 60% total blood volume, fluid resuscitation after 90 min). At onset of resuscitation, rats were treated with vehicle, E2, or E2 and estrogen receptor antagonist ICI 182,780 (ICI). A separate group of rats was treated with Ang II subtype I receptor (AT1R) antagonist losartan. At 24 h after T-H, plasma Ang II, IL-6, TNF-α, intercellular adhesion molecule (ICAM)-1, cytokine-induced neutrophil chemoattractant (CINC)-1 and CINC-3 levels, myeloperoxidase (MPO) activity, and AT1R expression were determined. T-H significantly increased plasma and intestinal Ang II, IL-6, TNF-α levels, intestinal ICAM-1, CINC-1, CINC-3 levels, MPO activity, and AT1R protein compared with shams. E2 treatment following T-H attenuated increased intestinal MPO activity, Ang II level, and AT1R protein expression. ICI administration abolished the salutary effects of E2. In contrast, losartan administration attenuated increased MPO activity without affecting Ang II and AT1R levels. Thus Ang II plays a role in producing small intestine inflammation following T-H, and the salutary effects of E2 on intestinal inflammation are mediated in part by Ang II and AT1R downregulation.

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CV-11974, angiotensin II type I receptor antagonist, protects against ischemia–reperfusion injury of the small intestine in rats

Cited by 22 publications

References 37 publications

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

Proinflammatory role of protease-activated receptor-2 in intestinal ischemia/reperfusion injury in rats

Estrogen prevents intestinal inflammation after trauma-hemorrhage via downregulation of angiotensin II and angiotensin II subtype I receptor

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